Abstract
CFTR, the cystic fibrosis transmembrane regulator, is a Cl− channel present in fetal alveolar epithelial cells where it contributes to Cl−, and thus fluid, secretion into the developing airspaces. At birth, the fetal lung converts from fluid secretion to fluid absorption. As the lung matures, CFTR expression decreases in the alveolar epithelium but remains prominent in the bronchiolar epithelium. Recently, CFTR has been shown to play an important role in fluid absorption in the distal airspaces of adult lung. The alveolar epithelium, the major site of fluid clearance in the lung, is composed of alveolar type I (TI) and type II (TII) cells, both of which contain sodium channels and Na+, K+-ATPase, by which active Na+ transport occurs. However, the routes for anion movement were unclear. CFTR has been demonstrated in adult TII cells, providing a means for Cl− transport. It is not known if CFTR is also present in TI cells, which cover >95% of the internal surface area of the lung. Hypothesis Alveolar TI cells contain CFTR, which may facilitate Cl− transport. Methods Immunohistochemistry and confocal microscopy were used to localize CFTR to specific alveolar epithelial cells in 2μ sections of adult rat lung and in cytocentrifuged preparations of isolated lung cells. Total RNA was extracted from isolated adult rat TI and TII cells and transcribed to cDNA. Quantitative PCR was performed using probes for CFTR and results were normalized to 18S. Results CFTR colocalizes to TI cells using immunohistochemistry. By QPCR analysis, both TI and TII cells contain mRNA for CFTR. Conclusion Alveolar TI cells contain CFTR, further implicating a role for TI cells in modulating lung fluid balance. Supported by RWJ Foundation and NIH Grants HL57426 and HL24075.
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